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The plasticizer di(2-ethylhexyl) phthalate (DEHP) is frequently detected in the environment due to the abundance of its use. These levels might be hazardous to human health and ecosystems. Phthalates have been associated with neurological disorders, yet whether chronic DEHP exposure plays a role in Parkinson's disease (PD) or its underlying mechanisms is unknown. We investigated the effects of chronic DEHP exposure less than an environmentally-relevant dose on PD hallmarks, using Caenorhabditis elegans as a model. We show that developmental stage and exposure timing influence DEHP-induced dopaminergic neuron degeneration. In addition, in response to chronic DEHP exposure at 5 mg/L, mitochondrial fragmentation became significantly elevated, reactive oxygen species (ROS) levels increased, and ATP levels decreased, suggesting that mitochondrial dysfunction occurs. Furthermore, the data show that mitochondrial complex I (nuo-1 and gas-1) and complex II (mev-1) are involved in DEHP-induced dopaminergic neuron toxicity. These results suggest that chronic exposure to DEHP at levels less than an environmentally-relevant dose causes dopaminergic neuron degeneration through mitochondrial dysfunction involving mitochondrial complex I and II. Considering the high level of genetic conservation between C. elegans and mammals, chronic DEHP exposure might elevate the risk of developing PD in humans.

Environmental nanoplastics (NPs) can accumulate in soils, posing a potential risk to soil ecosystems. However, the ecotoxicity of NPs for soil organisms has received little research attention. This study investigated whether NP exposure in soil leads to reproductive decline in the soil nematode Caenorhabditis elegans and sought to determine the mechanisms by which it may occur. Wild-type N2 C. elegans L1 larvae were exposed to various concentrations of nano-sized polystyrene (100 nm) in soil (0, 1, 10, 100, and 1000 mg/kg dry weight) for 96 h. We show that nano-sized polystyrene (100 nm) labeled with red fluorescence significantly accumulated in the intestine of C. elegans in a dose-dependent fashion via soil exposure (8%-47% increase). In addition, NP soil exposure led to 7%-33% decline in the number of eggs in utero and 2.6%-4.4% decline in the egg hatching percentage. We also find that the number of germ cell corpses (31%-55% increase) and the mRNA levels of germline apoptosis marker gene ced-3 (14%-31% increase) were significantly higher with greater NP soil exposure (10, 100, and 1000 mg/kg), while intracellular ATP levels were significantly reduced. Finally, the DEBtox model, which is based on the dynamic energy budget theory, was applied to show that the increased reproductive costs for C. elegans caused by NPs in soil are associated with energy depletion and reproductive decline. The threshold value (4.18 × 10

DEHP is commonly found in the environment, biota, food, and humans, raising significant health concerns. Whether developmental stage and exposure duration modify the obesogenic effects of DEHP is unclear, especially the underlying mechanisms by which chronic exposure to DEHP as well as its metabolites remain largely unknown. This study investigated the obesogenic effects of chronic DEHP exposure, with levels below environmentally-relevant amounts and provide the mechanism in Caenorhabditis elegans. We show that early-life DEHP exposure resulted in an increased lipid and triglyceride (TG) accumulation mainly attributed to DEHP itself, not its metabolite mono-2-ethylhexyl phthalate (MEHP). In addition, developmental stage and exposure timing influence DEHP-induced TG accumulation and chronic DEHP exposure resulted in the most significant effect. Analysis of fatty acid composition shows that chronic DEHP exposure altered fatty acid composition and TG, resulting in an increased ω-6/ω-3 ratio. The increased TG content by chronic DEHP exposure required lipogenic genes fat-6, fat-7, pod-2, fasn-1, and sbp-1. Moreover, chronic DEHP exposure induced XBP-1-mediated endoplasmic reticulum (ER) stress which might lead to up-regulation of sbp-1. This study suggests the possible involvement of ER stress and SBP-1/SREBP-mediated lipogenesis in chronic DEHP-induced obesogenic effects. Results from this study implies that chronic exposure to DEHP disrupts lipid metabolism, which is likely conserved across species due to evolutionary conservation of molecular mechanisms, raising concerns in ecological and human health.

Di(2-ethylhexyl)phthalate (DEHP) is an ubiquitous and emerging contaminant that is widely present in food, agricultural crop, and the environment, posing a potential risk to human health. This study utilized the nematode Caenorhabditis elegans to decipher the toxic effects of early life exposure to DEHP on aging and its underlying mechanisms. The results showed that exposure to DEHP at 0.1 and 1.5 mg/L inhibited locomotive behaviors. In addition, DEHP exposure significantly shortened the mean lifespan of the worms and further adversely affected pharyngeal pumping rate and defecation cycle in aged worms. Moreover, DEHP exposure also further enhanced accumulation of age-related biomarkers including lipofuscin, lipid peroxidation, and intracellular reactive oxygen species in aged worms. In addition, exposure to DEHP significantly suppressed gene expression of hsp-16.1, hsp-16.49, and hsp-70 in aged worms. Further evidences showed that mutation of genes involved in insulin/IGF-1-like signaling (IIS) pathway (daf-2, age-1, pdk-1, akt-1, akt-2, and daf-16) restored lipid peroxidation accumulation upon DEHP exposure in aged worms, whereas skn-1 mutation resulted in enhanced lipid peroxidation accumulation. Therefore, IIS and SKN-1 may serve as an important molecular basis for DEHP-induced age-related declines in C. elegans. Since IIS and SKN-1 are highly conserved among species, the age-related declines caused by DEHP exposure may not be exclusive in C. elegans, leading to adverse human health consequences due to widespread and persistent DEHP contamination in the environment.

Background: Parkinson's disease (PD) is a common neurodegenerative disease, yet fundamental treatments for the disease remain sparse. Thus, the search for potentially efficacious compounds from medicinal plants that can be used in the treatment of PD has gained significant interest. Purpose: In many medicinal plants, selenium is primarily found in an organic form. We investigated the neuroprotective potential of an organic form of selenium, N-γ-(L-glutamyl)-L-selenomethionine (Glu-SeMet) in a Caenorhabditis elegans PD model and its possible molecular mechanisms. Methods: We used a C. elegans pharmacological PD strain (BZ555) that specifically expresses green fluorescent protein (GFP) in dopaminergic neurons and a transgenic PD strain (NL5901) that expresses human α-synuclein (α-syn) in muscle cells to investigate the neuroprotective potential of Glu-SeMet against PD. Results: We found that Glu-SeMet significantly ameliorated 6-hydroxydopamine (6-OHDA)-induced dopaminergic neuron damage in the transgenic BZ555 strain, with corresponding improvements in slowing behavior and intracellular ROS levels. In addition, compared with clinical PD drugs (L-DOPA and selegiline), Glu-SeMet demonstrated stronger ameliorated effects on 6-OHDA-induced toxicity. Glu-SeMet also triggered the nuclear translocation of SKN-1/Nrf2 and significantly increased SKN-1, GST-4, and GCS-1 mRNA levels in the BZ555 strain. However, Glu-SeMet did not increase mRNA levels or ameliorate the damage to dopaminergic neurons when the BZ555 strain was subjected to skn-1 RNA interference (RNAi). Glu-SeMet also upregulated the mRNA levels of the selenoprotein TRXR-1 in both the BZ555 and BZ555; skn-1 RNAi strains and significantly decreased α-syn accumulation in the NL5901 strain, although this was not observed in the NL5901; trxr-1 strain. Conclusion: We found that Glu-SeMet has a neuroprotective effect against PD in a C. elegans PD model and that the anti-PD effects of Glu-SeMet were associated with SKN-1/Nrf2 and TRXR-1. Glu-SeMet may thus have the potential for use in therapeutic applications or supplements to slow the progression of PD.

Nanoplastic (NP) pollution is an emerging global concern due to its adverse impact on aquatic ecosystems. Nevertheless, the removal of aqueous NPs from aquatic environments remains a significant challenge. This study aims to investigate whether polystyrene NP in aqueous solutions can be removed using coffee grounds. Due to the difficulty associated with directly measuring NP levels and monitoring the biosorption process, we used fluorescent-orange amine-modified polystyrene beads (fluo-NP, 100 nm) to evaluate the efficacy of the biosorption process. The factors including pH, coffee grounds concentration, initial fluo-NP concentration, and contact time were optimized on batch experiments. In addition, the isotherm and kinetic models were employed to clarify the adsorption behaviors and mechanisms. It was found that aqueous fluo-NP particles were effectively adsorbed onto the coffee grounds over a wide pH range (pH 2–12), with a coffee ground concentration of 25 g/L leading to the maximum adsorption efficiency (74%). The equilibrium adsorption capacity of the coffee grounds was 4 mg/g for a reaction time of 40 min. Coffee grounds demonstrated the highest removal efficiency when the initial fluo-NP concentration was 100–125 mg/L. The Dubinin-Radushkevich model and pseudo-second-order model described the adsorption isotherm and kinetics well, respectively, and the adsorption at high fluo-NP concentration range was favorable. Moreover, the results suggest that the mechanism lies in the electrostatic interactions and hydrogen bonding between surface functional groups of the coffee grounds and the fluo-NP particles. Given that there is an urgent need to remove NPs from aqueous systems, this study illustrates that it is possible to use coffee ground biowaste for this purpose.

Manganese occurs naturally in sediment, yet anthropogenic sources, such as industrial wastewater and mining, increases Mn concentration. However, the environmental risk of bioavailable Mn is often overlooked and infrequently addressed. A probabilistic risk assessment was conducted to determine the effects of bioavailable Mn in river sediments on reproduction in model organism Caenorhabditis elegans using in utero egg counts and germline apoptosis as biomarkers. The lowest-observed-adverse-effect level (LOAEL) of sediment Mn that decreases in utero egg counts or increases germline apoptosis in C. elegans was 50 or 10 mg of Mn(II) per kg of dry weight sediment, respectively. Effect and exposure analyses were conducted using Hill model-simulated concentration-response curves and Mn concentrations of Laojie River sediment. Risk quotients (RQs) and exceedance risk (ER) analyses showed that bioavailable levels of Mn in Laojie River sediments from downstream sites collected during the dry season elevate reproductive risk as measured by germline apoptosis. These findings suggest that bioavailable levels of Mn in sediment exert negative impacts, and germline apoptosis is a sensitive biomarker for reproductive risk assessment. Our results also suggest that the anthropogenic Mn pollution in river sediment and spatial-seasonal bioavailability of Mn should be considered to improve sediment quality control.

Contamination by heavy metals and metalloids is a serious environmental and health concern. Acidic wastewaters are often associated with toxic metals which may enter and spread into agricultural soils. Several biological assays have been developed to detect toxic metals; however, most of them can only detect toxic metals in a neutral pH, not in an acidic environment. In this study, an acidophilic iron-oxidizing bacterium (IOB) Strain Y10 was isolated, characterized, and used to detect toxic metals toxicity in acidic water at pH 2.5. The colorimetric acidophilic IOB biosensor was based on the inhibition of the iron oxidizing ability of Strain Y10, an acidophilic iron-oxidizing bacterium, by metals toxicity. Our results showed that Strain Y10 is acidophilic iron-oxidizing bacterium. Thiobacillus caldus medium (TCM) (pH 2.5) supplied with both S4O62- and glucose was the optimum growth medium for Strain Y10. The optimum temperature and pH for the growth of Strain Y10 was 45 °C and pH 2.5, respectively. Our study demonstrates that the color-based acidophilic IOB biosensor can be semi-quantitatively observed by eye or quantitatively measured by spectrometer to detect toxicity from multiple toxic metals at pH 2.5 within 45 min. Our study shows that monitoring toxic metals in acidic water is possible by using the acidophilic IOB biosensor. Our study thus provides a novel approach for rapid and cost-effective detection of toxic metals in acidic conditions that can otherwise compromise current methods of chemical analysis. This method also allows for increased efficiency when screening large numbers of environmental samples.

Cadmium (Cd) contamination in sediment is an emerging concern for the sustainability of aquatic ecosystem due to the toxicity of Cd is correlated to different trophic levels. An effective and inexpensive remediation strategy for Cd-contaminated sediment is desirable. The feasibility of using a newly isolated acidophilic sulfur-oxidizing bacterium and untreated coffee ground to remediate Cd-contaminated sediment was evaluated. The bioleaching approach was firstly conducted with the acidophilic sulfur-oxidizing bacterial SV5, resulting in Cd(II) release from Cd(II)-contaminated sediment. Subsequently, Cd(II) in the acidic leachate was further removed using untreated agricultural wastes. Untreated coffee ground exhibited about 2-fold Cd(II) removal efficiency comparing to that of rice husk and peanut shell. Scanning electron microscope (SEM) and Fourier-transform infrared spectroscopy (FTIR) analysis were conducted to characterize the coffee ground after the adsorption of 0 or 200 mg/L Cd(II). At pH 4, the optimal coffee ground concentration was 30 g/L along with 100 mg/L Cd(II) concentration. Adsorption of Cd(II) by coffee ground was rapid and the adsorption kinetic followed pseudo-second order model. Cd(II) sorption by coffee ground was a favorable process and Langmuir isotherm model well described the experimental data. Taken together, even at pH 4, coffee ground still showed good biosorption capacity for Cd(II) with short equilibrium time. This study suggests that acidophilic sulfur-oxidizing bacterial SV5 and untreated coffee ground could be used as inexpensive and environment-friendly biomaterial and agricultural waste for the remediation of Cd-contaminated sediment.

The widespread use of di(2-ethylhexyl) phthalate (DEHP) has resulted in its ubiquitous presence in the environment, which has led to serious health concerns. One of these concerns is its possible link to Alzheimer’s disease (AD), which is the most common neurodegenerative disease in aged individuals. This study investigated whether early-life and chronic exposure to DEHP affects AD via the toxicity of amyloid-β (Aβ), which has been implicated in the pathogenesis of AD, using Caenorhabditis elegans AD models (strains CL4176 and CL2006). We show that early-life DEHP exposure increased Aβ toxicity in C. elegans strains CL4176 and CL2006. Early-life and chronic exposure to DEHP also significantly increased intracellular ROS levels and Aβ deposition in aged CL2006 nematodes. Moreover, it was found that DEHP-induced Aβ toxicity does not require transcription factors DAF-16 or SKN-1, while early-life and chronic exposure to DEHP significantly increased the accumulation of lysosome-related organelles and the mRNA levels of the autophagy-related gene bec-1 in aged CL2006 nematodes. Our findings suggest that early-life and chronic exposure to DEHP enhances Aβ toxicity, which may be associated with the autophagy–lysosomal degradation pathway in C. elegans.

The in vitro and in vivo antioxidant activities and its potential to protect against amyloid-P toxicity of essential oils from Zelkova serrata (Thunb.) Makino were investigated in the model organism Caenorhabditis elegans. The results revealed that the essential oil of Z serrata heartwood exhibited great radical scavenging activities and high total phenolic content. In vivo assays showed significant inhibition of oxidative damage in wild-type C. elegans under juglone- indueed oxidative stress and heat shock. Based on results from both in vitro and in vivo assays, the major compound in essential oil of heartwood, (-)-(S, 4S)- 7-hydroxycalamenene (IS, 4S-7HC), may contribute significantly to the observed antioxidant activity. Further evidence showed that IS, 4S-7HC significantly delayed the paralysis phenotype in amyloid beta-expressing transgenic C. elegans. These findings suggest that IS, 4S-7HC from the essential oil of Z serrata heartwood has potential as a source for antioxidant or Alzheimer's disease treatment.

Environmental nanomaterials contamination is a great concern for organisms including human. Copper oxide nanoparticles (CuO NPs) are widely used in a huge range of applications which might pose potential risk to organisms. This study investigated the in vivo transgenerational toxicity on development and reproduction with parental CuO NPs exposure in the nematode Caenorhabditis elegans. The results showed that CuO NPs (150 mg/L) significantly reduced the body length of parental C. elegans (P0). Only about 1 mg/L Cu2+ (~0.73%) were detected from 150 mg/L CuO NPs in 0.5X K-medium after 48 h. In transgenerational assays, CuO NPs (150 mg/L) parental exposure significantly induced developmental and reproductive toxicity in non-exposed C. elegans progeny (CuO NPs free) on body length (F1) and brood size (F1 and F2), respectively. In contrast, parental exposure to Cu2+ (1 mg/L) did not cause transgenerational toxicity on growth and reproduction. This suggests that the transgenerational toxicity was mostly attributed to the particulate form of CuO NPs. Moreover, qRT-PCR results showed that the mRNA levels of met-2 and spr-5 genes were significantly decreased at P0 and F1 upon only maternal exposure to CuO NPs (150 mg/L), suggesting the observed transgenerational toxicity was associated with possible epigenetic regulation in C. elegans.

River sediment is the ultimate sink for heavy metal pollution. Copper (Cu) and zinc (Zn) are consistently found at environmentally significant levels in sediments worldwide. We hypothesized that the bioavailability and potential ecological risk of Cu and Zn in river sediments may be affected by seasonal variations and spatial distribution. In this study, we tested our hypothesis using highly industrialized river sediments (Laojie River) as an example. The concentration of heavy metals, pollution indexes, and risk indexes were evaluated and multivariate statistical analyses were performed. We found that seasonal variations affect heavy metal contamination, pollution indexes, and potential ecological risk in sediments and this effect was more severe in the dry season. In addition, higher levels of metal contamination, pollution indexes, and potential ecological risk were observed midstream and downstream of the Laojie River. We found that Cu and Zn were the primary contaminants in Laojie River sediments and may originate from common anthropogenic sources. Analysis of the chemical fractions further revealed that Cu and Zn exhibited high mobility and potential bioavailability risk. In addition, a high percentage and amount of Cu and Zn were found in exchangeable fractions, suggesting they pose a great risk to aquatic organisms. Our results indicate that seasonal variations and spatial distribution affect the bioavailability and potential ecological risk of Cu and Zn in river sediments. These findings suggest that seasonal variations and spatial distribution are important parameters to consider for environmental monitoring and environmental management in aquatic environments.

Using arsenic (As) contaminated groundwater for drinking or irrigation has caused major health problems for humans around the world, raising a need to monitor As level efficiently and economically. This study developed a color-based bacterial biosensor which is easy-to-use and inexpensive for measuring As and could be complementary to current As detecting techniques. The arsR-lacZ recombinant gene cassette in nonpathogenic strain Escherichia coli DH5α was used in the color-based biosensor which could be observed by eyes or measured by spectrometer. The developed bacterial biosensor demonstrates a quantitative range from 10 to 500μgL(-1) of As in 3-h reaction time. Furthermore, the biosensor was able to successfully detect and estimate As concentration in groundwater sample by measuring optical density at 595nm (OD595). Among different storage methods used in this study, biosensor in liquid at 4°C showed the longest shelf life about 9d, and liquid storage at RT and cell pellet could also be stored for about 3-5d. In conclusion, this study showed that the As biosensor with reliable color signal and economical preservation methods is useful for rapid screening of As pollutant, providing the potential for large scale screening and better management strategies for environmental quality control.

The widespread use of zinc oxide nanoparticles (ZnO-NPs) has led to their release into the environment, and they thus represent a potential risk for both humans and ecosystems. However, the negative impact of ZnO-NPs on the immune system, especially in relation to host defense against pathogenic infection and its underlying regulatory mechanisms, remains largely unexplored. This study investigated the effects of early-life long-term ZnO-NPs exposure (from L1 larvae to adults) on innate immunity and its underlying mechanisms using a host–pathogen Caenorhabditis elegans model, and this was compared with the effect of ionic Zn. The results showed that the ZnO-NPs taken up by C. elegans primarily accumulated in the intestine and that early-life long-term ZnO-NPs exposure at environmentally relevant concentrations (50 and 500 μg/L) decreased the survival of wild-type C. elegans when faced with pathogenic Pseudomonas aeruginosa PA14 infection. Early-life long-term ZnO-NPs (500 μg/L) exposure significantly increased (by about 3-fold) the accumulation of live P. aeruginosa PA14 colonies in the intestine of C. elegans. In addition, ZnO-NPs (500 μg/L) inhibited the intestinal nuclear translocation of SKN-1 and also downregulated gcs-1 gene expression, which is an SKN-1 target gene. Further evidence revealed that early-life long-term exposure to ZnO-NPs (500 μg/L) did not increase susceptibility to mutation among the genes (pmk-1, sek-1, and nsy-1) encoding the p38 mitogen-activated protein kinase (MAPK) cascade in response to P. aeruginosa PA14 infection, though ZnO-NPs significantly decreased the mRNA levels of pmk-1, sek-1, and nsy-1. This study provides regulatory insight based on evidence that ZnO-NPs suppress the innate immunity of C. elegans and highlights the potential health risks of certain environmental nanomaterials, including ZnO-NPs, in terms of their immunotoxicity at environmentally relevant concentrations.

Background Parkinson's disease (PD) is a neurodegenerative disease that is associated with aging and is characterized as a movement disorder. Currently, there is still no complete therapy for PD. In recent years, the identification and characterization of medicinal plants to cure or treat PD has gained increasing scientific interest. Purpose In this study, we investigated a pentacyclic triterpenoid compound, β-amyrin, which is found in many medicinal plants for its anti-Parkinsonian effects, using Caenorhabditis elegans (C. elegans) disease models and their underlying mechanisms. Methods C. elegans treated or untreated with β-amyrin were investigated for oxidative stress resistance, neurodegeneration, and α-synuclein aggregation assays. The C. elegans ortholog of Atg8/LC3, LGG-1 that is involved in the autophagy pathway was also evaluated by quantitative RT-PCR and transgenic strain experiments. Results β-Amyrin exerted excellent antioxidant activity and reduced intracellular oxygen species in C. elegans. Using the transgenic strain BZ555, β-amyrin showed a protective effect on dopaminergic neurons reducing cell damage induced by 6-hydroxydopamine (6-OHDA). In addition, β-amyrin significantly reduced the α-synuclein aggregation in the transgenic strain NL5901. Moreover, β-amyrin up-regulated LGG-1 mRNA expression and increased the number of localized LGG-1 puncta in the transgenic strain DA2123. Conclusion The results from this study suggest that the anti-Parkinsonian effects of β-amyrin might be regulated via LGG-1 involved autophagy pathway in C. elegans. Therefore, β-amyrin may be useful for therapeutic applications or supplements to treat or slow the progression of PD.

ZnO nanoparticles (ZnO-NPs) are emerging contaminants that raise the concerns of potential risk in the aquatic environment. It has been estimated that the environmental ZnO-NPs concentration is 76 μg/l in the aquatic environment. Our aim was to determine the aquatic toxicity of ZnO-NPs with chronic exposure at environmentally relevant concentrations using the nematode Caenorhabditis elegans. Two simulated environmentally relevant mediums—moderately hard reconstituted water (EPA water) and simulated soil pore water (SSPW)—were used to represent surface water and pore water in sediment, respectively. The results showed that the ZnO-NPs in EPA water has a much smaller hydrodynamic diameter than that in SSPW. Although the ionic release of Zn ions increased time-dependently in both mediums, the Zn ions concentrations in EPA water increased two-fold more than that in SSPW at 48 h and 72 h. The ZnO-NPs did not induce growth defects or decrease head thrashes in C. elegans in either media. However, chronic exposure to ZnO-NPs caused a significant reduction in C. elegans body bends in EPA water even with a relatively low concentration (0.05 μg/l); similar results were not observed in SSPW. Moreover, at the same concentrations (50 and 500 μg/l), body bends in C. elegans were reduced more severely in ZnO-NPs than in ZnCl2 in EPA water. The ATP levels were consistently and significantly decreased, and ROS was induced after ZnO-NPs exposure (50 and 500 μg/l) in EPA water. Our results provide evidences that chronic exposure to ZnO-NPs under environmentally relevant concentrations causes metabolic and locomotive toxicities implicating the potential ecotoxicity of ZnO-NPs at low concentrations in aquatic environments.

// Kumar K.J. Senthil 1 , Vani M. Gokila 1,2 , Jeng-Leun Mau 2,3 , Chin-Chung Lin 4 , Fang-Hua Chu 5 , Chia-Cheng Wei 6 , Vivian Hsiu-Chuan Liao 6 and Sheng-Yang Wang 1,2,7 1 Department of Forestry, National Chung Hsing University, Taichung, Taiwan 2 National Chung Hsing University/University of California at Davis, Plant and Food Biotechnology Center, National Chung Hsing University, Taichung, Taiwan 3 Department of Food Science and Biotechnology, National Chung Hsing University, Taichung, Taiwan 4 Taiwan Leader Biotech Company, Taipei, Taiwan 5 School of Forestry and Resource Conservation, National Taiwan University, Taipei, Taiwan 6 Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan 7 Agricultural Biotechnology Research Center, Academia Sinica, Taipei, Taiwan Correspondence to: Sheng-Yang Wang, email: // Keywords : Antcin M, antrodia salmonea , hyperglycemia, stress-induced premature senescence, SIRT-1, Gerotarget Received : February 18, 2016 Accepted : July 27, 2016 Published : August 11, 2016 Abstract The present study revealed the anti-aging properties of antcin M (ANM) and elucidated the molecular mechanism underlying the effects. We found that exposure of human normal dermal fibroblasts (HNDFs) to high-glucose (HG, 30 mM) for 3 days, accelerated G 0 /G 1 phase arrest and senescence. Indeed, co-treatment with ANM (10 µM) significantly attenuated HG-induced growth arrest and promoted cell proliferation. Further molecular analysis revealed that ANM blocked the HG-induced reduction in G 1 -S transition regulatory proteins such as cyclin D, cyclin E, CDK4, CDK6, CDK2 and protein retinoblastoma (pRb). In addition, treatment with ANM eliminated HG-induced reactive oxygen species (ROS) through the induction of anti-oxidant genes, HO-1 and NQO-1 via transcriptional activation of Nrf2. Moreover, treatment with ANM abolished HG-induced SIPS as evidenced by reduced senescence-associated β-galactosidase (SA-β-gal) activity. This effect was further confirmed by reduction in senescence-associated marker proteins including, p21 CIP1 , p16 INK4A , and p53/FoxO1 acetylation. Also, the HG-induced decline in aging-related marker protein SMP30 was rescued by ANM. Furthermore, treatment with ANM increased SIRT-1 expression, and prevented SIRT-1 depletion. This protection was consistent with inhibition of SIRT-1 phosphorylation at Ser47 followed by blocking its upstream kinases, p38 MAPK and JNK/SAPK. Further analysis revealed that ANM partially protected HG-induced senescence in SIRT-1 silenced cells. A similar effect was also observed in Nrf2 silenced cells. However, a complete loss of protection was observed in both Nrf2 and SIRT-1 knockdown cells suggesting that both induction of Nrf2-mediated anti-oxidant defense and SIRT-1-mediated deacetylation activity contribute to the anti-aging properties of ANM in vitro . Result of in vivo studies shows that ANM-treated C. elegens exhibits an increased survival rate during HG-induced oxidative stress insult. Furthermore, ANM significantly extended the life span of C. elegans . Taken together, our results suggest the potential application of ANM in age-related diseases or as a preventive reagent against aging process.

Microbially mediated dissolution of iron oxyhydroxides plays a defining role in the arsenic (As) release in most reducing environments, though the nature of this relationship remain unclear. This study aimed to evaluate the microbial processes on the enhancement or inhibition of As release as a function of bacterial enrichments from groundwater and core sediments. Two enrichment cultures of reducing bacteria (RB) used were cultivated from core sediment (RB-S) and groundwater (RB-W). The microcosm experiments were systematically conducted to assess microbially mediated reactions for the mobility of As from sediment into groundwater. From the analysis results, simultaneous bioreduction of As and Fe contributed to the initial elevation of aqueous As. Distinct distribution patterns of aqueous As and Fe between RW-S and RB-W revealed the different microbial activities. RB-W showed strong affinity for solid As, leading to high level of aqueous As. In contrast, RB-S exhibited high reducing ability toward Fe minerals, and the following formation of secondary Fe-As minerals constrained dissolved As. By amending with non-sterile groundwater, we also observed the chelating solubilization of As-contained Fe minerals, leading to the increase of As(III) and Fe(III). This comparative study illustrates the distinct function of indigenous metal-reducing microbes cultured from groundwater and sediment in liberating aquifer As and Fe. Our results provide evidence that the release and sequestration of As are closely related to specific microbial population in aquifer. The limitation of bioavailability of As and carbon source further influences the release of As to groundwater.

Monascin is a major yellow compound from red mold dioscorea. We investigated monascin to test whether this compound acts as an antidiabetic and antioxidative stress agent in diabetic rats and Caenorhabditis elegans. The mechanisms by which monascin exerts its action in vivo were also examined. Streptozotocin (STZ)-induced diabetic rats were given monascin at 30 mg/kg/day and sacrificed after 8 weeks. Blood glucose and serum insulin, triglyceride, total cholesterol, and high-density lipoprotein and antioxidative enzymes in the pancreas of rats were measured. In addition, monascin was evaluated for stress resistance and potential associated mechanisms in C. elegans. Throughout the 8-week experimental period, significantly lowered blood glucose, serum triglyceride, and total cholesterol and higher high-density lipoprotein levels were observed in monascin-treated rats. Monascin-treated rats showed higher serum insulin level, lower reactive oxygen species production, and higher activities of glutathione peroxidase, superoxide dismutase, and catalase in the pancreas compared to diabetic control rats. In addition, monascin significantly induced the hepatic mRNA levels of FOXO3a, FOXO1, MnSOD, and catalase in STZ-induced diabetic rats. Monascin-treated C. elegans showed an increased survival rate during oxidative stress and heat stress treatments compared to untreated controls. Moreover, monascin extended the life span under high-glucose conditions and enhanced expression of small heat shock protein (sHSP-16.2), superoxide dismutase (SOD-3), and glutathione S-transferase (GST-4) in C. elegans. Finally, we showed that monascin affected the subcellular distribution of the FOXO transcription factor DAF-16, whereas it was unable to enhance oxidative stress resistance in the daf-16 deletion mutant in C. elegans. Mechanistic studies in rats and C. elegans suggest that the protective effects of monascin are mediated via regulation of the FOXO/DAF-16-dependent insulin signaling pathway by inducing the expression of stress response/antioxidant genes, thereby enhancing oxidative stress resistance.

Arsenic is a known human carcinogen and high levels of arsenic contamination in food, soils, water, and air are of toxicology concerns. Nowadays, arsenic is still a contaminant of emerging interest, yet the effects of arsenic on aging process have received little attention. In this study, we investigated the effects and the underlying mechanisms of chronic arsenite exposure on the aging process in Caenorhabditis elegans. The results showed that prolonged arsenite exposure caused significantly decreased lifespan compared to non-exposed ones. In addition, arsenite exposure (100 μM) caused significant changes of age-dependent biomarkers, including a decrease of defecation frequency, accumulations of intestinal lipofuscin and lipid peroxidation in an age-dependent manner in C. elegans. Further evidence revealed that intracellular reactive oxygen species (ROS) level was significantly increased in an age-dependent manner upon 100 μM arsenite exposure. Moreover, the mRNA levels of transcriptional makers of aging (hsp-16.1, hsp-16.49, and hsp-70) were increased in aged worms under arsenite exposure (100 μM). Finally, we showed that daf-16 mutant worms were more sensitive to arsenite exposure (100 μM) on lifespan and failed to induce the expression of its target gene sod-3 in aged daf-16 mutant under arsenite exposure (100 μM). Our study demonstrated that chronic arsenite exposure resulted in accelerated aging process in C. elegans. The overproduction of intracellular ROS and the transcription factor DAF-16/FOXO play roles in mediating the accelerated aging process by arsenite exposure in C. elegans. This study implicates a potential ecotoxicological and health risk of arsenic in the environment.

Curcumin is the active ingredient in the herbal medicine and dietary spice, turmeric (Curcuma longa). It has a wide range of biological activities, including anti-inflammatory, antioxidant, chemopreventive, and chemotherapeutic activities. We examined the effects of curcumin on the lifespan and aging in Caenorhabditis elegans, and found that it responded to curcumin with an increased lifespan and reduced intracellular reactive oxygen species and lipofuscin during aging. We analyzed factors that might influence lifespan extension by curcumin. We showed that lifespan extension by curcumin in C. elegans is attributed to its antioxidative properties but not its antimicrobial properties. Moreover, we showed that lifespan extension had effects on body size and the pharyngeal pumping rate but not on reproduction. Finally, lifespan tests with selected stress- and lifespan-relevant mutant strains revealed that the lifespan-extending phenotype was absent from the osr-1, sek-1, mek-1, skn-1, unc-43, sir-2.1, and age-1 mutants, whereas curcumin treatment prolonged the lifespan of mev-1 and daf-16 mutants. Our study has unraveled a diversity of modes of action and signaling pathways to longevity and aging with curcumin exposure in vivo.

Drinking highly arsenic-contaminated groundwater is a likely cause of blackfoot disease in Taiwan, but microorganisms that potentially control arsenic mobility in the subsurface remain unstudied. The objective of this study was to investigate the relevant arsenite-oxidizing and arsenate-reducing microbial community that exists in highly arsenic-contaminated groundwater in Taiwan. We cultured and identified arsenic-transforming bacteria, analyzed arsenic resistance and transformation, and determined the presence of genetic markers for arsenic transformation. In total, 11 arsenic-transforming bacterial strains with different colony morphologies and varying arsenic transformation abilities were isolated, including 10 facultative anaerobic arsenate-reducing bacteria and one strictly aerobic arsenite-oxidizing bacterium. All of the isolates exhibited high levels of arsenic resistance with minimum inhibitory concentrations of arsenic ranging from 2 to 200 mM. Strain AR-11 was able to rapidly oxidize arsenite to arsenate at concentrations relevant to environmental groundwater samples without the addition of any electron donors or acceptors. We provide evidence that arsenic-reduction activity may be conferred by the ars operon(s) that were not amplified by the designed primers currently in use. The 16S rRNA sequence analysis grouped the isolates into the following genera: Pseudomonas, Bacillus, Psychrobacter, Vibrio, Citrobacter, Enterobacter, and Bosea. Among these genera, we present the first report of the genus Psychrobacter being involved in arsenic reduction. Our results further support the hypothesis that bacteria capable of either oxidizing arsenite or reducing arsenate coexist and are ubiquitous in arsenic-contaminated groundwater.

Selenium is an essential trace nutrient that has a narrow exposure window between its beneficial and detrimental effects. We investigated how selenium affected the development, fertility, and cholinergic signaling of the nematode, Caenorhabditis elegans. Our results showed that selenite supplementation at 0.01 and 0.05 μM accelerated development and increased the brood size, while the addition of 20 μM selenite retarded the developmental rate and decreased the brood size. We also showed that the 0.01 μM selenite-pretreated nematodes were more resistant to paralysis induced by an acetylcholinesterase inhibitor, aldicarb, and a nicotinic acetylcholine receptor agonist, levamisole, compared to untreated worms. In contrast, 20 μM selenite-pretreated animals were more sensitive to aldicarb- and levamisole-induced paralysis compared to untreated worms. We measured the internal selenium in supplemented worms using inductively coupled plasma atomic emission spectroscopy, and the data obtained suggested that selenite added to growth medium was taken up by the worms. Taken together, these results suggest that selenite exerts both ameliorative and toxic effects on C.elegans, depending on the amount. Our investigations here thus reinforce our understanding of the ameliorative and toxic effects of selenium on development, reproduction, and cholinergic signaling.

This work characterized the sink and source/mobility of As in the As-affected sedimentary aquifers of the southern Choushui River alluvial fan, central Taiwan. Major mineral phases and chemical components were determined by XRD and X-ray photoelectron spectroscopy (XPS). The partitioning of As and Fe among cores were determined by sequential extraction. Based on XPS results, the primary forms of Fe were hematite, goethite and magnetite. Sequential extraction data and the XRF analysis indicated that Fe oxyhydroxides and sulfides were likely to be the major sinks of As, particularly in the distal-fan. Furthermore, Fe oxyhydroxides retained higher As contents than As-bearing sulfides. The reductive dissolution of Fe oxyhydroxides, which accompanied high levels of HCO 3 - and NH 4 + concentrations, was likely the principal release mechanism of As into groundwater in this area. The dual roles of Fe oxyhydroxides which are governed by the local redox condition act as a sink and source in the aquifer. Ionic replacement by PO 4 3 - and HCO 3 - along with seasonal water table fluctuation, caused by monsoons and excessive pumping, contributed specific parts of As in the groundwater. The findings can be used to account for the inconsistency between Fe and As concentrations observed in groundwater.

Endotoxin, a component of gram-negative bacterial cell walls, is a proinflammatory agent that induces local and systemic inflammatory responses in normal subjects which can contribute to the risk of developing asthma and chronic obstructive lung diseases. A probabilistic approach linking models of exposure, internal dosimetry, and health effects were carried out to quantitatively assess the potential inhalation risk of airborne endotoxin for workers in cotton textile plants. Combining empirical data and modeling results, we show that the half-maximum effects of the endotoxin dose (ED50) were estimated to be 3.3 x 10(5) (95% confidence interval (CI): 1.9-14.7 x 10(5)) endotoxin units (EU) for the blood C-reactive protein (CRP) concentration, 1.1 x 10(5) (95% CI: 0.6-1.7 x 10(5))EU for the blood polymorphonuclear neutrophil (PMN) count, and 1.5 x 10(5) (95% CI: 0.4-2.5 x 10(5))EU for the sputum PMN count. Our study offers a risk-management framework for discussing future establishment of limits for respiratory exposure to airborne endotoxin for workers in cotton textile plants.

Environmental pollution with petroleum products such as benzene, toluene, ethylbenzene, and xylenes (BTEX) has garnered increasing awareness because of its serious consequences for human health and the environment. We have constructed toluene bacterial biosensors comprised of two reporter genes, gfp and luxCDABE, characterized by green fluorescence and luminescence, respectively, and compared their abilities to detect bioavailable toluene and related compounds. The bacterial luminescence biosensor allowed faster and more-sensitive detection of toluene; the fluorescence biosensor strain was much more stable and thus more applicable for long-term exposure. Both luminescence and fluorescence biosensors were field-tested to measure the relative bioavailability of BTEX in contaminated groundwater and soil samples. The estimated BTEX concentrations determined by the luminescence and fluorescence bacterial biosensors were closely comparable to each other. Our results demonstrate that both bacterial luminescence and fluorescence biosensors are useful in determining the presence and the bioavailable fractions of BTEX in the environment.

A computational model was developed to examine the phototriggered folding of a caged protein, a protein modified with an organic photolabile cross-linker. Molecular dynamics simulations of the modified 36-residue fragment of subdomain B of chicken villin head piece with a photolabile linker were performed, starting from both the caged and the uncaged structures. Construction of a free-energy landscape, based on principal components as well as on radius of gyration versus root-mean-square deviation, and circular dichroism calculations were employed to characterize folding behavior and structures. The folded structures observed in the molecular dynamics trajectories were found to be similar to that of the wild-type protein, in agreement with the published experimental results. The free-energy landscapes of the modified and wild-type proteins have similar topology, suggesting common thermodynamic/kinetic behavior. The existence of small differences in the free-energy surface of the modified protein from that of the native protein, however, indicates subtle differences in the folding behavior.

The lethal concentration for 50% of aquacultural animals (LC50)-based tests determines the external effect concentration (EEC) following certain statistical models, revealing that no biologically based mechanistic information and only statistical interpretations of its model parameters could be made. The purpose of this paper is to determine the survival risk of waterborne metals toward farmed species with respect to lethality based on biologically based mechanistic models. Here we study a biologically based mechanistic damage assessment model (DAM) compared with a pharmacodynamic (PD)-based critical area under the curve (CAUC) model to demonstrate the ability of predicting the internal effect concentration (IEC) and survival rate of farmed species. We tested the proposed models using published acute toxicity and accumulation data for two farmed species, tilapia (Orechromis mossambicus) exposed to arsenic (As) and abalone (Haliotis diversicolor supertexta) exposed to zinc (Zn), to compare observed and predicted LC50 and IEC and, subsequently, to predict the survival rate. Our analyses demonstrate that the DAM- and PD-based survival models performed well and proved its usefulness as a tool in the quantification of risk assessment in aquacultural ecosystems. The study also supports the suggestion that replacing exposure-based EECs by IECs is a first step toward a measure for inherent toxicity and can be used to improve the construction of future environmental quality criteria programs aimed at protecting and restoring the rapidly degrading aquacultural ecosystems.

Cadmium is an environmental contaminant that is both a human toxicant and carcinogen. To inhibit cadmium-induced damage, cells respond by increasing the expression of genes that encode stress-response proteins. We previously reported the identification of 48 cadmium-inducible mRNAs in the nematode Caenorhabditis elegans. Here we describe a new cadmium-responsive gene, designated cdr-1, whose rate and level of inducible expression parallel those of the C. elegans metallothioneins. The CDR-1 mRNA contains an open reading frame of 831 bp and encodes a predicted 32-kDa, integral membrane protein. Following cadmium exposure, cdr-1 is transcribed exclusively in intestinal cells of post-embryonic C. elegans. In vivo, the CDR-1 protein is targeted specifically to the intestinal cell lysosomes. cdr-1 transcription is significantly induced by cadmium but not by other tested stressors. These results indicate that cdr-1 expression is regulated by cadmium and in a cell-specific fashion. Inhibition of CDR-1 expression renders C. elegans susceptible to cadmium toxicity. In conclusion, cdr-1 defines a new class of cadmium-inducible genes and encodes an integral membrane, lysosomal protein. This protein functions to protect against cadmium toxicity.

The transition metal cadmium is a pervasive and persistent environmental contaminant that has been shown to be both a human toxicant and carcinogen. To inhibit cadmium-induced damage, cells respond by increasing the expression of genes encoding stress-response proteins. In most cases, the mechanism by which cadmium affects the expression of these genes remains unknown. It has been demonstrated in several instances that cadmium activates gene transcription through signal transduction pathways, mediated by protein kinase C, cAMP-dependent protein kinase, or calmodulin. A codicil is that cadmium should influence the expression of numerous genes. To investigate the ability of cadmium to affect gene transcription, the differential display technique was used to analyze gene expression in the nematode Caenorhabditis elegans. Forty-nine cDNAs whose steady-state levels of expression change 2–6-fold in response to cadmium exposure were identified. The nucleotide sequences of the majority of the differentially expressed cDNAs are identical to those of C. elegans cosmids, yeast artificial chromosomes, expressed sequence tags, or predicted genes. The translated amino acid sequences of several clones are identical to C. elegansmetallothionein-1, HSP70, collagens, and rRNAs. In addition, C. elegans homologues of pyruvate carboxylase, DNA gyrase, β-adrenergic receptor kinase, and human hypothetical protein KIAA0174 were identified. The translated amino acid sequences of the remaining differentially expressed cDNAs encode novel proteins.

Arsenic (As) contamination of groundwater is a significant public health concern. In this study, the removal of arsenic from groundwater using biological processes was investigated. The efficiency of arsenite (As(III)) bacterial oxidation and subsequent arsenate (As(V)) removal from contaminated groundwater using bacterial biomass was examined. A novel As(III)-oxidizing bacterium (As7325) was isolated from the aquifer in the blackfoot disease (BFD) endemic area in Taiwan. As7325 oxidized 2300μg/l As(III) using in situ As(III)-contaminated groundwater under aerobic conditions within 1d. After the oxidation of As(III) to As(V), As(V) removal was further examined using As7325 cell pellets. The results showed that As(V) could be adsorbed efficiently by lyophilized As7325 cell pellets, the efficiency of which was related to lyophilized cell pellet concentration. Our study conducted the examination of an alternative technology for the removal of As(III) and As(V) from groundwater, indicating that the oxidation of As(III)-contaminated groundwater by native isolated bacterium, followed by As(V) removal using bacterial biomass is a potentially effective technology for the treatment of As(III)-contaminated groundwater.

BACKGROUND: Phthalate esters are ubiquitous environmental contaminants and numerous organisms are thus exposed to various levels of phthalates in their natural habitat. Considering the critical, but limited, research on human neurobehavioral outcomes in association with phthalates exposure, we used the nematode Caenorhabditis elegans as an in vivo model to evaluate phthalates-induced neurotoxicity and the possible associated mechanisms. PRINCIPAL FINDINGS: Exposure to phthalates (DEHP, DBP, and DIBP) at the examined concentrations induced behavioral defects, including changes in body bending, head thrashing, reversal frequency, and thermotaxis in C. elegans. Moreover, phthalates (DEHP, DBP, and DIBP) exposure caused toxicity, affecting the relative sizes of cell body fluorescent puncta, and relative intensities of cell bodies in AFD neurons. The mRNA levels of the majority of the genes (TTX-1, TAX-2, TAX-4, and CEH-14) that are required for the differentiation and function of AFD neurons were decreased upon DEHP exposure. Furthermore, phthalates (DEHP, DBP, and DIBP) exposure at the examined concentrations produced elevated intracellular reactive oxygen species (ROS) in C. elegans. Finally, pretreatment with the antioxidant ascorbic acid significantly lowered the intracellular ROS level, ameliorated the locomotor and thermotactic behavior defects, and protected the damage of AFD neurons by DEHP exposure. CONCLUSIONS: Our study suggests that oxidative stress plays a critical role in the phthalate esters-induced neurotoxic effects in C. elegans.

The in vitro and in vivo antioxidant activities and its potential to protect against amyloid-β toxicity of essential oils from Zelkova serrata (Thunb.) Makino were investigated in the model organism Caenorhabditis elegans. The results revealed that the essential oil of Z. serrata heartwood exhibited great radical scavenging activities and high total phenolic content. In vivo assays showed significant inhibition of oxidative damage in wild-type C. elegans under juglone-induced oxidative stress and heat shock. Based on results from both in vitro and in vivo assays, the major compound in essential oil of heartwood, (-)-(1 S, 4 S)-7-hydroxycalamenene (1 S, 4 S-7HC), may contribute significantly to the observed antioxidant activity. Further evidence showed that 1 S, 4 S-7HC significantly delayed the paralysis phenotype in amyloid beta-expressing transgenic C. elegans. These findings suggest that 1 S, 4 S-7HC from the essential oil of Z. serrata heartwood has potential as a source for antioxidant or Alzheimer's disease treatment.

Cinnamomum osmophloeum Kaneh is an indigenous tree species in Taiwan. In this study, phytochemical characteristics and antioxidant activities of the essential oils and key constituents from the leaves of two C. osmophloeum clones were investigated. The two trees possess two chemotypes, which were classified as the cinnamaldehyde type and camphor type. We demonstrated that the essential oils from C. osmophloeum leaves exerted in vivo antioxidant activities in Caenorhabditis elegans. In addition, trans-cinnamaldehyde and D-(+)-camphor, which respectively represent the major compounds in the cinnamaldehyde-type and camphor-type trees, exerted significant in vivo antioxidant activities against juglone-induced oxidative stress in C. elegans. Moreover, expressions of antioxidative-related genes, including superoxide dismutase (SOD) and glutathione S-transferase (GST), were significantly induced by trans-cinnamaldehyde and D-(+)-camphor from C. osmophloeum leaves. Our results showed that the essential oils from C. osmophloeum leaves and their major compounds might have good potential for further development as nutraceuticals or antioxidant remedies.

High levels of arsenic in groundwater and drinking water represent a major health problem worldwide. Drinking arsenic-contaminated groundwater is a likely cause of blackfoot disease (BFD) in Taiwan, but mechanisms controlling the mobilization of arsenic present at elevated concentrations within aquifers remain understudied. Microcosm experiments using sediments from arsenic contaminated shallow alluvial aquifers in the blackfoot disease endemic area showed simultaneous microbial reduction of Fe(III) and As(V). Significant soluble Fe(II) (0.23 ± 0.03 mM) in pore waters and mobilization of As(III) (206.7 ± 21.2 nM) occurred during the first week. Aqueous Fe(II) and As(III) respectively reached concentrations of 0.27 ± 0.01 mM and 571.4 ± 63.3 nM after 8 weeks. We also showed that the addition of acetate caused a further increase in aqueous Fe(II) but the dissolved arsenic did not increase. We further isolated an As(V)-reducing bacterium native to aquifer sediments which showed that the direct enzymatic reduction of As(V) to the potentially more-soluble As(III) in pore water is possible in this aquifer. Our results provide evidence that microorganisms can mediate the release of sedimentary arsenic to groundwater in this region and the capacity for arsenic release was not limited by the availability of electron donors in the sediments.

Exposures to carcinogenic polycyclic aromatic hydrocarbons (PAHs) have been linked to human lung cancer. The purpose of this study was to assess lung cancer risk caused by inhalation exposure to nano/ultrafine particle-bound PAHs at the population level in Taiwan appraised with recent published data. A human respiratory tract model was linked with a physiologically based pharmacokinetic model to estimate deposition fraction and internal organic-specific PAHs doses. A probabilistic risk assessment framework was developed to estimate potential lung cancer risk. We reanalyzed particle size distribution, total-PAHs, particle-bound benzo(a)pyrene (B[a]P) and PM concentrations. A dose-response profile describing the relationships between external B[a]P concentration and lung cancer risk response was constructed based on population attributable fraction (PAF). We found that 90% probability lung cancer risks ranged from 10(-5) to 10(-4) for traffic-related nano and ultrafine particle-bound PAHs, indicating a potential lung cancer risk. The particle size-specific PAF-based excess annual lung cancer incidence rate due to PAHs exposure was estimated to be less than 1 per 100,000 population, indicating a mild risk factor for lung cancer. We concluded that probabilistic risk assessment linked PAF for limiting cumulative PAHs emissions to reduce lung cancer risk plays a prominent role in future government risk assessment program.

Redox couples approach and multivariate statistical techniques, including factor analysis, cluster analysis and discriminant analysis, were applied to evaluate and to interpret the complex groundwater quality in the blackfoot disease endemic area, Taiwan. Most groundwater samples were characterized as Na-Ca-HCO(3) with HCO(3)(-) as the dominant anion. Total arsenic (As) concentration, predominantly as As(3+), ranged from1.0 to 562.7 μg/L. The patterns of measured reducing potential were consistent with those values calculated from As couple, revealing the in situ environment enhanced the accumulation of As concentration in the groundwater. Factor analysis proposed a four-factor model, comprising salination, reductive dissolution of Fe/Mn oxyhydroxides, As reduction and chemical potential factor, and explained 89.94% of total variance in groundwater. Furthermore, two factors, reductive dissolution of Fe/Mn oxyhydroxides and As reduction, suggested that the decoupled reductive processes accounted for high As concentration in this area. Cluster analysis was adopted to spatially categorize the sampled wells into three main clusters and characterized by the factor scores of the four-factor model. Two-parameter (pH and Eh) model derived from discriminant analysis can be used for preliminary assessment to determine whether the As concentration exceeds 10 μg/L with simple field measurements in this area.

Endotoxin, a component of gram-negative bacterial cell walls, is a pro-inflammatory agent that induces local and systemic inflammatory responses in normal subjects which can contribute to the risk of developing asthma and chronic obstructive lung diseases. A probabilistic approach linking models of exposure, internal dosimetry, and health effects was carried out to quantitatively assess the potential inhalation risk of airborne endotoxin in homes during the winter and summer seasons. Combining empirical data and modeling results, we show that the half-maximum effect of the endotoxin dose (ED50) was estimated to be 707.9 (95% confidence interval (CI): 308.8-1287.0) endotoxin units (EU) for body temperature change, 481.8 (95% CI: 333.2-630.3) EU for elevation of neutrophils, and 1174.5 (95% CI: 816.0-1532.9) EU for elevation of the cytokine, interleukin-6. Our study also suggests that airborne endotoxin in homes may pose potential risks, and a higher risk for elevation of neutrophils and cytokine interleukin-6 appeared in winter season than in summer. Our study offers a risk-management framework for discussion of future studies of human respiratory exposure to airborne endotoxin.

We developed an inductance-based valvometry technique as a detection system to measure the valve daily activity in freshwater clam Corbicula fluminea in response to waterborne arsenic. Our findings reveal that C. fluminea experiences a valve opening in the absence of arsenic predominantly in the morning hours (03:00-08:00) with a mean daily opening/closing period of 21.32 (95% CI: 20.58-22.05) h. Amplification of daily activity occurred in the presence of arsenic. Behavioral toxicity assays revealed arsenic detection thresholds of 0.60 (95% CI: 0.53-0.66) mg l(-1) and 0.35 (95% CI: 0.30-0.40) mg l(-1) for response times of 60 and 300 min, respectively. The proposed valve daily activity model was linked with response time-specific Hill dose-response functions to predict valve opening/closing behavior in response to arsenic. The predictive capabilities were verified satisfactory with the measurements. Our results implicate a biomonitoring system by valve daily activity in C. fluminea to identify safe water uses in areas with elevated arsenic.

Arsenic is a potent human carcinogen of skin, lung, and urinary bladder. Freshwater clam Corbicula fluminea is a commercially important native species in Taiwan. C. fluminea is also a suitable biomonitoring test organism. Little is known, however, about the actual effects of arsenic on C. fluminea. The objectives of this study were to provide information on the acute toxicity and bioaccumulation kinetics of arsenic in C. fluminea. We carried out a 14-day exposure experiment to obtain bioaccumulation parameters. Uptake was very rapid when C. fluminea was first exposed and then slightly decayed during the uptake phase of the experiment and an uptake rate constant of 1.718 +/- 6.70 (mean +/- SE) mL g(-1) d(-1) was estimated. The elimination of arsenic from C. fluminea obeyed first-order depuration kinetics (r(2) = 0.85, p < 0.05) with a calculated half-life of 6.80 days. The derived bioaccumulation factor of 16.84 suggests that arsenic has a high potential for bioaccumulation in C. fluminea. This had important implications for dietary exposure of arsenic to humans who eat contaminated clams, because the soft tissue usually constitutes the majority of tissue consumed. The 96-h LC50 value was estimated to be 20.74 (95% CI: 11.74-30.79) mg L(-1) obtained from a 7-day acute toxicity bioassay. We also kinetically linked an acute toxicity model and a Hill sigmoid model to reconstruct an internal effect concentration based dose-response profile to assess the effect of soft tissue arsenic burden on the C. fluminea mortality. This result could be used to support the establishment of an ecological risk assessment to prevent possible ecosystem and human health consequences.